Alterations induced by E-cadherin and β-catenin antibodies during the development of Bufo arenarum (Anura-Bufonidae)

Abstract

E(epithelia1)-cadherin is a member of a calcium-dependent family of cell surface glycoproteins involved in cell-cell adhesion and morphogenesis. Catenins are a large family of proteins that connect the cadherins to the cytoskeleton. They are important for cadherin function and for transducing signals involved in specification of cell fate during embryogenesis. The best characterized catenins include α-, β-, ɣ-, and p120- catenin. Using specific antibodies, we studied the expression and distribution of E-cadherin, and a- and β-catenin in developmental stages of Bufo arenarum toad. The three proteins were found CO-localized in stages 19 to 41 of development. Surprisingly, E-cadherin was the only of these three proteins found earlier than stage 19. To test whether E-cadherin and β-catenin have a functional role in Bufo arenarum embryogenesis, stage 17 whole embryos were incubated with anti-E-cadherin and β-catenin antibodies. Both anti-E-cadherin and anti- β-catenin antibodies induced severe morphological alterations. However, while alterations produced by the anti-β-catenin antibody, showed some variability from the most severe (neural tube and notochord duplication) to a simple delay in development, the alterations with anti-E-cadherin were homogeneous. These observations suggest a critical role for E-cadherin and β-catenin in the early embryonic development of the Bufo arenarum toad. Our results are consistent with the developmental role of these proteins in other species. One of the most surprising findings was the blockage with the anti-β-catenin antibodies on later embryo stages, and we hypothesize that the partial axes duplication could be mediated by the notochord induction.